tbuckley/cabot-search huggingface dataset:
Concurrent pembrolizumab with AVD for untreated classical Hodgkin lymphoma
Authors: Ryan C Lynch, Chaitra S Ujjani, Christina Poh, Edus H Warren, Stephen D Smith, Mazyar Shadman, Brian G. Till, Vikram Raghunathan, Stefan Alig, Ash A Alizadeh, Avanti Gulhane, Delphine Chen, Yolanda Tseng, Hilary Coye, Megan Shelby, Susan Ottemiller, Sarith Keo, Kaitlin Verni, Hongyan Du, Jacquelin Vandermeer, Ashley Gaston, Heather Rasmussen, Paul Martin, Edmond Marzbani, Jenna M Voutsinas, Ajay K Gopal
Journal: Blood (2023)
Bioelectronic Sensor Nodes for the Internet of Bodies
Authors: Baibhab Chatterjee, Pedram Mohseni, Shreyas Sen
Journal: Annual Review of Biomedical Engineering (2023)

Energy-efficient sensing with physically secure communication for biosensors on, around, and within the human body is a major area of research for the development of low-cost health care devices, enabling continuous monitoring and/or secure perpetual operation. When used as a network of nodes, these devices form the Internet of Bodies, which poses challenges including stringent resource constraints, simultaneous sensing and communication, and security vulnerabilities. Another major challenge is to find an efficient on-body energy-harvesting method to support the sensing, communication, and security submodules. Due to limitations in the amount of energy harvested, we require a reduction in energy consumed per unit information, making the use of in-sensor analytics and processing imperative. In this article, we review the challenges and opportunities of low-power sensing, processing, and communication with possible powering modalities for future biosensor nodes. Specifically, we analyze, compare, and contrast (a) different sensing mechanisms such as voltage/current domain versus time domain, (b) low-power, secure communication modalities including wireless techniques and human body communication, and (c) different powering techniques for wearable devices and implants.
Why COP28 must be a health COP
Authors: Emma L Lawrance, Mala Rao
Journal: BMJ (2023)

The start of the year is a time of reflection, of looking forward to the future and resolving to make life changes with positive improvements.Making resolutions is important and worthwhile; it signals the optimism that a better future is possible and can inspire others to join shared goals.Our reflections this year were rather different, with 2022 ending with our attendance at the United Nations' Conference of Parties' COP27 summit.Wandering through the cacophony of noise and myriad pavilions-where nearly 50 000 participants congregated, making it the largest COP to date-was extraordinarily energising.
Advances in Injectable Hydrogel Strategies for Heart Failure Treatment
Authors: Shuyi He, Zaiyuan Zhang, Rifang Luo, Qing Jiang, Li Yang, Yunbing Wang
Journal: Advanced Healthcare Materials (2023)

Heart failure (HF) affects 60 million people worldwide and has developed into a global public health problem surpassing cancer and urgently needs to be solved. According to the etiological spectrum, HF due to myocardial infarction (MI) has become the dominant cause of morbidity and mortality. Possible treatments include pharmacology, medical device implantation, and cardiac transplantation, which are limited in their ability to promote long-term functional stabilization of the heart. Injectable hydrogel therapy has emerged as a minimally invasive tissue engineering treatment approach. Hydrogels can provide the necessary mechanical support for the infarcted myocardium and serve as carriers of various drugs, bioactive factors, and cells to improve the cellular microenvironment in the infarcted region and induce myocardial tissue regeneration. Herein, the pathophysiological mechanism of HF is explored and injectable hydrogels as a potential solution for current clinical trials and applications are summarized. Specifically, mechanical support hydrogels, decellularized ECM hydrogels, a variety of biotherapeutic agent-loaded hydrogels and conductive hydrogels for cardiac repair were discussed, and the mechanism of action of these hydrogel-based therapies was emphasized. Finally, the limitations and future prospects of injectable hydrogel therapy for HF post MI were proposed to inspire novel therapeutic strategies.
Cardiac Arrest During Delivery Hospitalization
Authors: Nicole D. Ford, Carla L. DeSisto, Romeo R. Galang, Elena V. Kuklina, Laurence S. Sperling, Jean Y. Ko
Journal: Annals of Internal Medicine (2023)

Estimates of cardiac arrest occurring during delivery guide evidence-based strategies to reduce pregnancy-related death.To investigate rate of, maternal characteristics associated with, and survival after cardiac arrest during delivery hospitalization.Retrospective cohort study.U.S. acute care hospitals, 2017 to 2019.Delivery hospitalizations among women aged 12 to 55 years included in the National Inpatient Sample database.Delivery hospitalizations, cardiac arrest, underlying medical conditions, obstetric outcomes, and severe maternal complications were identified using codes from the International Classification of Diseases, 10th Revision, Clinical Modification. Survival to hospital discharge was based on discharge disposition.Among 10 921 784 U.S. delivery hospitalizations, the cardiac arrest rate was 13.4 per 100 000. Of the 1465 patients who had cardiac arrest, 68.6% (95% CI, 63.2% to 74.0%) survived to hospital discharge. Cardiac arrest was more common among patients who were older, were non-Hispanic Black, had Medicare or Medicaid, or had underlying medical conditions. Acute respiratory distress syndrome was the most common co-occurring diagnosis (56.0% [CI, 50.2% to 61.7%]). Among co-occurring procedures or interventions examined, mechanical ventilation was the most common (53.2% [CI, 47.5% to 59.0%]). The rate of survival to hospital discharge after cardiac arrest was lower with co-occurring disseminated intravascular coagulation (DIC) without or with transfusion (50.0% [CI, 35.8% to 64.2%] or 54.3% [CI, 39.2% to 69.5%], respectively).Cardiac arrests occurring outside delivery hospitalizations were not included. The temporality of arrest relative to the delivery or other maternal complications is unknown. Data do not distinguish cause of cardiac arrest, such as pregnancy-related complications or other underlying causes among pregnant women.Cardiac arrest was observed in approximately 1 in 9000 delivery hospitalizations, among which nearly 7 in 10 women survived to hospital discharge. Survival was lowest during hospitalizations with co-occurring DIC.None.
Correction: Anticipatory changes in British household purchases of soft drinks associated with the announcement of the Soft Drinks Industry Levy: A controlled interrupted time series analysis
Authors: Nina T. Rogers, David Pell, Tarra L. Penney, Oliver Mytton, Adam Briggs, Steven Cummins, Mike Rayner, Harry Rutter, Peter Scarborough, Stephen J. Sharp, Richard D. Smith, Martin White, Jean Adams
Journal: PLoS Medicine (2023)

[This corrects the article DOI: 10.1371/journal.pmed.1003269.].
Surgery in Early Metastatic Seminoma: A Phase II Trial of Retroperitoneal Lymph Node Dissection for Testicular Seminoma With Limited Retroperitoneal Lymphadenopathy
Authors: Siamak Daneshmand, Clint Cary, Timothy Masterson, Lawrence Einhorn, Nabil Adra, Stephen A. Boorjian, Christian Kollmannsberger, Anne Schuckman, Alan So, Peter Black, Aditya Bagrodia, Eila Skinner, Mehrdad Alemozaffar, Timothy Brand, Scott Eggener, Phillip Pierorazio, Kelly Stratton, Lucia Nappi, Craig Nichols, Chunqiao Luo, Ming Li, Brian Hu
Journal: Journal of Clinical Oncology (2023)

The long-term toxicities of chemotherapy and radiotherapy can represent a significant burden to testicular cancer survivors. Retroperitoneal lymph node dissection (RPLND) is an established treatment for testicular germ cell tumors with minimal late morbidity although little data exist on its efficacy in early metastatic seminoma. Surgery in early metastatic seminoma is a prospective phase II single-arm, multi-institutional trial of RPLND as first-line treatment for testicular seminoma with clinically low-volume retroperitoneal lymphadenopathy.
Contrast-Induced Acute Kidney Injury and Cardiovascular Imaging: Danger or Distraction?
Authors: Matthew S. Davenport, Mark A. Perazella, Brahmajee K. Nallamothu
Journal: Circulation (2023)

2020, the American College of Radiology and the National Kidney Foundation released consensus statements declaring the prevalence of contrast-induced acute kidney injury (CI-AKI) to be much lower than historically reported. 1This guideline concluded that most CI-AKI from intravenous contrast medium administration is not caused by contrast medium, but instead by coincident nephrotoxic exposures. 1,2It was a dramatic shift in thinking.Just 2 decades earlier, in 2002, CI-AKI was believed to be the third most common cause of hospital-acquired AKI. 3 However, modern evidence indicated that such prevalence estimates were biased and overstated, as nearly all the literature on CI-AKI lacked adequate control groups. 1,2,4onsidering this, the term contrast-associated AKI (CA-AKI) was noted to be preferred over CI-AKI for labeling AKI that occurs after contrast exposure when the cause is unknown. 1 Regardless of cause, AKI continued to be defined using accepted Kidney Disease Improving Global Outcomes criteria: increase in serum creatinine ≥0.3 mg/dL within 48 hours, increase in serum creatinine ≥1.5-fold within 7 days, or urine volume <0.5 mL•kg -1 •h -1 for 6 hours. 1 Clinicians who image patients with kidney disease outside cardiology have reacted appropriately, and radiology guidelines have been revised worldwide.Screening with serum creatinine is no longer routinely performed in patients undergoing noncardiac imaging without known kidney disease.Contrast-enhanced computed tomography (CT) is now performed without prophylaxis in most patients with a stable estimated glomerular filtration rate (eGFR) ≥30 mL•min -1 •1.73 m -2 , and necessary contrast-enhanced CT is now performed irrespective of risk of CI-AKI if there is no reasonable alternative.
Perm1 Protects the Heart From Pressure Overload–Induced Dysfunction by Promoting Oxidative Metabolism
Authors: Shizuko Tachibana, Nam-Kyung Yu, Ruixia Li, Carolina Fernandez-Costa, Alex Liang, Janet Choi, Dayoen Jung, Changchun Xiao, Anastasia Kralli, John R. Yates, Robert S. Ross, Yoshitake Cho
Journal: Circulation (2023)
Efficacy of Osimertinib in Patients with Lung Cancer Positive for Uncommon EGFR Exon 19 Deletion Mutations
Authors: Michael J. Grant, Jacqueline V. Aredo, Jacqueline H. Starrett, Paul Stockhammer, Iris K. van Alderwerelt van Rosenburgh, Anna Wurtz, Andrew J. Piper-Valillo, Zofia Piotrowska, Christina Falcon, Helena A. Yu, Charu Aggarwal, Dylan Scholes, Tejas Patil, Christina Nguyen, Manali Phadke, Fang-Yong Li, Joel Neal, Mark A. Lemmon, Zenta Walther, Katerina Politi, Sarah B. Goldberg
Journal: Clinical Cancer Research (2023)

Abstract Purpose: The uncommon EGFR exon 19 deletion (ex19del), L747_A750&amp;gt;P, demonstrates reduced sensitivity to osimertinib compared with the common ex19del, E746_A750del in preclinical models. The clinical efficacy of osimertinib in patients with non–small cell lung cancer harboring L747_A750&amp;gt;P and other uncommon ex19dels is not known. Experimental Design: The AACR GENIE database was interrogated to characterize the frequency of individual ex19dels relative to other variants, and a multicenter retrospective cohort was used to compare clinical outcomes for patients with tumors harboring E746_A750del, L747_A750&amp;gt;P, and other uncommon ex19dels who received osimertinib in the first line (1L) or in second or later lines of therapy and were T790M+ (≥2L). Results: ex19dels comprised 45% of EGFR mutations, with 72 distinct variants ranging in frequency from 28.1% (E746_A750del) to 0.03%, with L747_A750&amp;gt;P representing 1.8% of the EGFR mutant cohort. In our multi-institutional cohort (N = 200), E746_A750del was associated with significantly prolonged progression-free survival (PFS) with 1L osimertinib versus L747_A750&amp;gt;P [median 21.3 months (95% confidence interval, 17.0–31.7) vs. 11.7 months (10.8–29.4); adjusted HR 0.52 (0.28–0.98); P = 0.043]. Osimertinib efficacy in patients with other uncommon ex19dels varied on the basis of the specific mutation present. Conclusions: The ex19del L747_A750&amp;gt;P is associated with inferior PFS compared with the common E746_A750del mutation in patients treated with 1L osimertinib. Understanding differences in osimertinib efficacy among EGFR ex19del subtypes could alter management of these patients in the future.
SOX17 Deficiency Mediates Pulmonary Hypertension: At the Crossroads of Sex, Metabolism, and Genetics
Authors: Shreya Sangam, Xutong Sun, Tae-Hwi Schwantes-An, Manivannan Yegambaram, Qing Lu, Yinan Shi, Todd Cook, Amanda Fisher, Andrea L. Frump, Anna Coleman, Yanan Sun, Shuxin Liang, Howard Crawford, Katie A. Lutz, Avinash D. Maun, Michael W. Pauciulo, Jason H. Karnes, Ketul R. Chaudhary, Duncan J. Stewart, Paul R. Langlais, Mohit Jain, Mona Alotaibi, Tim Lahm, Yan Jin, Haiwei Gu, Haiyang Tang, William C. Nichols, Stephen M. Black, Ankit A. Desai
Journal: American Journal of Respiratory and Critical Care Medicine (2023)

Rationale: Genetic studies suggest that SOX17 (SRY-related HMG-box 17) deficiency increases pulmonary arterial hypertension (PAH) risk. Objectives: On the basis of pathological roles of estrogen and HIF2α (hypoxia-inducible factor 2α) signaling in pulmonary artery endothelial cells (PAECs), we hypothesized that SOX17 is a target of estrogen signaling that promotes mitochondrial function and attenuates PAH development via HIF2α inhibition. Methods: We used metabolic (Seahorse) and promoter luciferase assays in PAECs together with the chronic hypoxia murine model to test the hypothesis. Measurements and Main Results: Sox17 expression was reduced in PAH tissues (rodent models and from patients). Chronic hypoxic pulmonary hypertension was exacerbated by mice with conditional Tie2-Sox17 (Sox17EC−/−) deletion and attenuated by transgenic Tie2-Sox17 overexpression (Sox17Tg). On the basis of untargeted proteomics, metabolism was the top pathway altered by SOX17 deficiency in PAECs. Mechanistically, we found that HIF2α concentrations were increased in the lungs of Sox17EC−/− and reduced in those from Sox17Tg mice. Increased SOX17 promoted oxidative phosphorylation and mitochondrial function in PAECs, which were partly attenuated by HIF2α overexpression. Rat lungs in males displayed higher Sox17 expression versus females, suggesting repression by estrogen signaling. Supporting 16α-hydroxyestrone (16αOHE; a pathologic estrogen metabolite)–mediated repression of SOX17 promoter activity, Sox17Tg mice attenuated 16αOHE-mediated exacerbations of chronic hypoxic pulmonary hypertension. Finally, in adjusted analyses in patients with PAH, we report novel associations between a SOX17 risk variant, rs10103692, and reduced plasma citrate concentrations (n = 1,326). Conclusions: Cumulatively, SOX17 promotes mitochondrial bioenergetics and attenuates PAH, in part, via inhibition of HIF2α. 16αOHE mediates PAH development via downregulation of SOX17, linking sexual dimorphism and SOX17 genetics in PAH.
Pharmacology and Clinical Development of Factor XI Inhibitors
Authors: Antonio Greco, Claudio Laudani, Marco Spagnolo, Federica Agnello, Denise Cristiana Faro, Simone Finocchiaro, Marco Legnazzi, Maria Sara Mauro, Placido Maria Mazzone, Giovanni Occhipinti, Carla Rochira, Lorenzo Scalia, Davide Capodanno
Journal: Circulation (2023)

Therapeutic anticoagulation is indicated for a variety of circumstances and conditions in several fields of medicine to prevent or treat venous and arterial thromboembolism. According to the different mechanisms of action, the available parenteral and oral anticoagulant drugs share the common principle of hampering or blocking key steps of the coagulation cascade, which unavoidably comes at the price of an increased propensity to bleed. Hemorrhagic complications affect patient prognosis both directly and indirectly (ie, by preventing the adoption of an effective antithrombotic strategy). Inhibition of factor XI (FXI) has emerged as a strategy with the potential to uncouple the pharmacological effect and the adverse events of anticoagulant therapy. This observation is based on the differential contribution of FXI to thrombus amplification, in which it plays a major role, and hemostasis, in which it plays an ancillary role in final clot consolidation. Several agents were developed to inhibit FXI at different stages (ie, suppressing biosynthesis, preventing zymogen activation, or impeding the biological action of the active form), including antisense oligonucleotides, monoclonal antibodies, small synthetic molecules, natural peptides, and aptamers. Phase 2 studies of different classes of FXI inhibitors in orthopedic surgery suggested that dose-dependent reductions in thrombotic complications are not paralleled by dose-dependent increases in bleeding compared with low-molecular-weight heparin. Likewise, the FXI inhibitor asundexian was associated with lower rates of bleeding compared with the activated factor X inhibitor apixaban in patients with atrial fibrillation, although no evidence of a therapeutic effect on stroke prevention is available so far. FXI inhibition could also be appealing for patients with other conditions, including end-stage renal disease, noncardioembolic stroke, or acute myocardial infarction, for which other phase 2 studies have been conducted. The balance between thromboprophylaxis and bleeding achieved by FXI inhibitors needs confirmation in large-scale phase 3 clinical trials powered for clinical end points. Several of such trials are ongoing or planned to define the role of FXI inhibitors in clinical practice and to clarify which FXI inhibitor may be most suited for each clinical indication. This article reviews the rationale, pharmacology, results of medium or small phase 2 studies, and future perspectives of drugs inhibiting FXI.
Annals Graphic Medicine - Opinion: Someone Does Not Belong
Authors: Rachel Weber
Journal: Annals of Internal Medicine (2023)

Web ExclusivesMarch 2023Annals Graphic Medicine - Opinion: Someone Does Not BelongFREERachel Weber, BSRachel Weber, BSMedical College of Wisconsin, Wauwatosa, Wisconsin (R.W.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/G22-0036 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Download figure Download PowerPoint Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAuthors: Rachel Weber, BSAffiliations: Medical College of Wisconsin, Wauwatosa, Wisconsin (R.W.)Disclosures: The author has reported no disclosures of interest. The form can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=G22-0036.Author/Illustrator Information: Rachel Weber, BS, is an MD candidate, class of 2024, and an aspiring surgeon. To see more of her work, visit www.rachelweberartworkportfolio.com (e-mail, [email protected]edu).This article was published at Annals.org on 14 March 2023. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics March 2023Volume 176, Issue 3 ePublished: 14 March 2023 Issue Published: March 2023 Copyright & PermissionsCopyright © 2023 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Effect of Yoga on Frailty in Older Adults
Authors: Julia Loewenthal, Kim E. Innes, Margalit Mitzner, Carol Mita, Ariela R. Orkaby
Journal: Annals of Internal Medicine (2023)

Background: Yoga, a multicomponent mind–body practice, improves several domains of physical and psychological health and may affect frailty in older adults. Purpose: To evaluate the available trial evidence on the effect of yoga-based interventions on frailty in older adults. Data Sources: MEDLINE, EMBASE, and Cochrane Central from their inception to 12 December 2022. Study Selection: Randomized controlled trials evaluating the effect of yoga-based interventions, including at least 1 session of physical postures, on a validated frailty scale or single-item markers of frailty in adults aged 65 years or older. Data Extraction: Two authors independently screened articles and extracted data; 1 author assessed risk of bias with review from a second author. Disagreements were resolved through consensus and as-needed input from a third author. Data Synthesis: Thirty-three studies (n = 2384 participants) were identified in varied populations, including community dwellers, nursing home residents, and those with chronic disease. Yoga styles were primarily based on Hatha yoga and most often included Iyengar or chair-based methods. Single-item frailty markers included measures of gait speed, handgrip strength, balance, lower-extremity strength and endurance, and multicomponent physical performance measures; no studies included a validated definition of frailty. When compared with education or inactive control, there was moderate-certainty evidence that yoga improved gait speed and lower-extremity strength and endurance, low-certainty evidence for balance and multicomponent physical function measures, and very low-certainty evidence for handgrip strength. Limitation: Heterogeneity in study design and yoga style, small sample sizes, and reporting deficiencies leading to concerns for selection bias. Conclusion: Yoga may affect frailty markers that are associated with clinically meaningful outcomes in older adult populations but may not offer benefit over active interventions (for example, exercise). Primary Funding Source: None. (PROSPERO: CRD42020130303)
Cardiac Amyloidosis
Authors: Michelle Weisfelner Bloom, Peter D. Gorevic
Journal: Annals of Internal Medicine (2023)

Amyloidosis is a pathologic and clinical condition resulting from the accumulation of insoluble aggregates of misfolded proteins in tissues. Extracellular deposition of amyloid fibrils in the myocardium leads to cardiac amyloidosis, which is often overlooked as a cause of diastolic heart failure. Although cardiac amyloidosis was previously believed to have a poor prognosis, recent advances in diagnosis and treatment have emphasized the importance of early recognition and changed management of this condition. This article provides an overview of cardiac amyloidosis and summarizes current screening, diagnosis, evaluation, and treatment options.
Harnessing cell-material interactions to control stem cell secretion for osteoarthritis treatment
Authors: Nathan Lagneau, Pierre Tournier, Fabien Nativel, Yves Maugars, Jérôme Guicheux, Catherine Le Visage, Vianney Delplace
Journal: Biomaterials (2023)

Osteoarthritis (OA) is the most common debilitating joint disease, yet there is no curative treatment for OA to date. Delivering mesenchymal stromal cells (MSCs) as therapeutic cells to mitigate the inflammatory symptoms associated with OA is attracting increasing attention. In principle, MSCs could respond to the pro-inflammatory microenvironment of an OA joint by the secretion of anti-inflammatory, anti-apoptotic, immunomodulatory and pro-regenerative factors, therefore limiting pain, as well as the disease development. However, the microenvironment of MSCs is known to greatly affect their survival and bioactivity, and using tailored biomaterial scaffolds could be key to the success of intra-articular MSC-based therapies. The aim of this review is to identify and discuss essential characteristics of biomaterial scaffolds to best promote MSC secretory functions in the context of OA. First, a brief introduction to the OA physiopathology is provided, followed by an overview of the MSC secretory functions, as well as the current limitations of MSC-based therapy. Then, we review the current knowledge on the effects of cell-material interactions on MSC secretion. These considerations allow us to define rational guidelines for next-generation biomaterial design to improve the MSC-based therapy of OA.